Abstract
Young albino rabbits were administered 5, 10, 20, and 50 mg of sodium fluoride/kg body weight/day subcutaneously for 3.5 months. The control animals were given 1 mL of double distilled water/kg body weight/day. In the fluoridated rabbits, the myocardium showed cloudy swellings, sarcoplasmic vacuolization, and small hemorrhages followed by fibrous necrosis. The degenerative changes were most pronounced in animals treated with 50 mg of sodium fluoride/kg body weight/day. The myocardium exhibited fibrous necrosis, dissolution of nuclei, fibrillolysis, extensive vacuole formation and interstitial cells in the connective tissue. The degree of myocardial damage seemed to be directly proportional to the dosage of fluoride administered. In the control animals, the myocardium showed normal structure without any of the changes mentioned above.
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Aortic calcification in chronic fluoride poisoning: biochemical and electronmicroscopic evidence
Fluoride is known to cause ectopic calcification. The biochemical mechanism(s) involved in the initiation of calcification is not understood and the accompanying ultrastructural changes remain to be elucidated. Therefore, certain relevant parameters have been investigated in the aorta of rabbits administered fluoride, 10 mg NaF/kg body wt, every 24 hr
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Ca2+ metabolic disorder and abnormal expression of cardiac troponin involved in fluoride-induced cardiomyocyte damage.
Highlights F induced cardiomyocyte damage. F induced Ca2+ metabolic disorder. F inhibited the expression of cardiac troponin. F induced ultrastructure damage in cardiomyocytes. F interfered with production of ATP in cardiomyocytes. Our previous study indicated that excessive fluoride (F) induces ATP5J and ATP5H proactive expression by interfering cardiomyocyte mitochondrial dysfunction in
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Effects of chronic ingestion of sodium fluoride on myocardium in a second generation of rats
Possible effects of long term exposure (6 months) to sodium fluoride (NaF) through drinking water on the morphology and biochemistry of myocardial tissue in second generation adult male rats were investigated. Wistar strain female and male rats were reared until the second generation of rats obtained, during which they were
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Fluoride-induced oxidative stress in rat myocardium through the Bax/Bcl-2 signalling pathway
The purpose of this study was to investigate whether fluoride (F) induces cardiotoxicity in rats and to discuss its underlying mechanisms by detecting morphological change, enzyme activity of oxidative stress, and the expression of Bcl-2 family protein. With increasing dosages of F, obvious pathological changes occurred in the myocardial tissue
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ITRAQ-based proteomics reveals the potential mechanism of fluoride-induced myocardial contraction function damage.
Highlights Pressure-volume loop analysis highlighted the impaired effects of fluoride exposure on cardiac function and myocardial contraction indicators. Histological analysis of rat heart tissue under fluoride exposure revealed extensive damage. Proteomics analysis highlighted effects on the myocardial contraction pathway. Protein network analysis highlighted the key roles of RyRs, Tpm and
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Structural damage to the heart resulting from fluoride toxicity has been observed in numerous human and animal studies. The general features of this damage include cloudy swelling, vacuolization or vacuolar degeneration, hemorrhages, interstitial edema, fibrous necrosis, dissolution of nuclei, and thickening of the vessel walls in the heart muscle (Basha
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